Since a previous study suggested that AML patients with an immune-enriched tumor microenvironment, as supported by the detection of an increased expression of genes associated with CD8 lymphocytes, B cells and Th1 cells, CXCL9 and CXCL10, are less likely to respond to anthracycline-based cytotoxic chemotherapy and have a shorter relapse-free survival [141], it was hypothesized that the presence of an immune-enriched gene signature in the bone marrow of AML patients more likely to respond to flotetuzumab-based immunotherapy [142]. The gene discussed is CXCL10; the disease is acute myeloid leukemia.